Bian Di, Chen Yi-guo, Sui Yue-jiao, Tian Hui, Liu Yu-li, Cao Rui, Li Cheng-lin, Li Bao-yan
Zhen Ci Yan Jiu. 2015 Feb;40(1):45-9.
To observe the effect of electroacupuncture (EA) stimulation of "Neiguan" (PC 6) on expression of sodium (Nav) channel α-subunit 1.5 and Nav β-subunits β 1-β 4 (the known myocardial sodium channel proteins) in acute myocardial ischemia (AMI) rats so as to explore its mechanisms underlying protection of ischemic myocardium.
Sixty SD male rats were randomly divided into normal control, AMI model, Neiguan (PC 6), Lieque (LU 7) and non-acupoint groups. The AMI model was established by intravenous injection of Isoprenaline (85 mg/kg) once daily for 2 days. Myocardial Nav 1.5 and Nav β 1, β 2, β 3, β 4 protein expression levels were detected by Western blot.
In comparison with the control group, myocardial Nav 1.5, β 1, β 2, β 3 and β 4 protein expression levels were significantly down-regulated in the AMI model group (P<0.01). After EA stimulation, compared with the model group, the expression levels of Nav 1.5, Nav β 1, β 2, β 3 and β 4 protein expression levels were significantly up-regulated in the Neiguang (PC 6) and Lieque (LU 7) groups (P<0.01) rather than in the non-acupoint group (P>0.05). There was no statistical significance between the Neiguan (PC 6) and Lieque (LU 7) groups in β 4 protein expression level (P>0.05).
EA stimulation of both PC 6 and LU 7 can significantly reverse AMI-induced down-regulation of myocardial Nav 1.5, β 1, β 2, β 3 and β 4 protein expression levels in AMI rats, which might contribute to its function in improving AMI by reducing calcium overload.
观察电针刺激“内关”(PC 6)对急性心肌缺血(AMI)大鼠心肌钠(Nav)通道α亚基1.5及Nav β亚基β1-β4(已知的心肌钠通道蛋白)表达的影响,以探讨其保护缺血心肌的机制。
将60只雄性SD大鼠随机分为正常对照组、AMI模型组、内关(PC 6)组、列缺(LU 7)组和非穴位组。通过每日静脉注射异丙肾上腺素(85 mg/kg),连续2天建立AMI模型。采用蛋白质免疫印迹法检测心肌Nav 1.5及Nav β1、β2、β3、β4蛋白表达水平。
与对照组相比,AMI模型组心肌Nav 1.5、β1、β2、β3及β4蛋白表达水平显著下调(P<0.01)。电针刺激后,与模型组相比,内关(PC 6)组和列缺(LU 7)组Nav 1.5、Nav β1、β2、β3及β4蛋白表达水平显著上调(P<0.01),而非穴位组无明显变化(P>0.05)。内关(PC 6)组与列缺(LU 7)组β4蛋白表达水平比较,差异无统计学意义(P>0.05)。
电针刺激PC 6和LU 7均可显著逆转AMI大鼠心肌Nav 1.5、β1、β2、β3及β4蛋白表达水平的下调,这可能是其通过减轻钙超载改善AMI的作用机制之一。